DOCSLIB.ORG

ECG-In-The-Athlete.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
ECG-In-The-Athlete.Pdf Electrocardiogram in the Athlete Joint Session ISE-FIAI-SOLAECE-SIAC ICE 2015 Comandatuba, Bahia, Brazil Martín Ibarrola MD, FAHA Centro Cardiovascular BV Director of Medical Department of Sports Rugby and Hockey. Club Regatas de Bella Vista Argentina Pre-participation screening can prevent sudden cardiac death in the athletes ▪Medical history: ➢Personal history. ➢Family history ➢Physical examination ▪ ECG changes that would be considered abnormal in the untrained population may develop in trained athletes as a physiologic and benign consequence of the heart's adaptation to exercise. Italian program ▪ Young competitive athletes aged 12 to 35 years are included. ▪ 2 consecutive screening periods (1982-1992and1993-2004) in Italian program. The number of competitive athletes aged 12 to 35 years in the Veneto region from 1982 to 2004 was 42 386 athletes Interpretation of ECG in athlete’s ▪ 12-lead ECG in the athlete: physiological versus pathological abnormalities. Review. Br J Sports Med 2009. Corrado D. MD; et al. ▪ Recommendations for interpretation of 12-lead electrocardiogram in the athlete. ESC REPORT. European Heart Journal 2010. Corrado D. MD; et al. ▪ Interpretation of the Electrocardiogram of Young Athletes. Special Report. Uberoi A. MD; et al. Circulation 2011 ▪ Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’. Br J Sports Med 2013. Drezner J A; et al. Refinement of the European Society of Cardiology (ESC) criteria ▪ Improving the interpretation of the athlete’s electrocardiogram. EDITORIAL. Corrado D. el al. European Heart Journal 2013 European Society of Cardiology (ESC) classification of ECG abnormalities in athletes Recommendations for interpretation of 12-lead electrocardiogram in the athlete Group 1: common and Group 2: uncommon and training-related ECG training-unrelated ECG changes (>80%) changes (<5%) ▪ Sinus bradycardia ▪ T-wave inversion ▪ First-degree AV block ▪ ST-segment depression ▪ Incomplete RBBB ▪ Pathological Q-waves ▪ Early repolarization ▪ Left atrial enlargement ▪ Left-axis deviation/left anterior ▪ Isolated QRS voltage hemiblock criteria for left ventricular ▪ Right-axis deviation/left posterior hypertrophy hemiblock ▪ Right ventricular hypertrophy ▪ Ventricular pre-excitation ▪ Complete LBBB or RBBB ▪ Long- or short-QT interval ▪ Brugada-like early repolarization Domenico Corrado, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. European Heart Journal (2010) 31, 243–259 The ‘Seattle Criteria’: Electrocardiographic interpretation in athletes (1) Normal ECG findings in athletes Abnormal ECG findings in athletes (1) T-wave inversion >1 mm in depth in two or more leads V2–V6, II and aVF, or I and 1. Sinus bradycardia (≥ 30 bpm) aVL (excludes III, aVR and V1) 2. Sinus arrhythmia ST segment depression ≥0.5 mm in depth in two or more leads Pathologic Q waves >3 mm in depth or >40 ms in duration in two or more leads 3. Ectopic atrial rhythm (except for III and aVR) 4. Junctional escape rhythm Complete left bundle branch block QRS ≥120 ms, predominantly negative QRS complex in lead V1 (QS or rS), and upright monophasic R wave in leads I and V6 5. 1° AV block (PR interval > 200 ms) Intraventricular conduction delay. Any QRS duration ≥140 ms 6. Mobitz Type I (Wenckebach) 2° AV block Left axis deviation −30° to −90° Left atrial enlargement Prolonged P wave duration of >120 ms in leads I or II with 7. Incomplete RBBB negative portion of the P wave ≥1 mm in ventricular hypedepth and ≥40 ms in duration 8. Isolated QRS voltage criteria for LVH in lead V1 Right hipertrophy pattern ▸ Except: QRS voltage criteria for LVH occurring R−V1+S−V5>10.5 mm AND right axis deviation >120° with Ventricular pre-excitation PR interval <120 ms with a delta wave (slurred upstroke in any non-voltage criteria for LVH such as left the QRS complex) and wide QRS (>120 ms) Long QT interval* atrial QTc≥470 ms (male) enlargement, left axis deviation, ST segment QTc≥480 ms (female) depression, T-wave inversion or pathological QTc≥500 ms (marked QT prolongation) Short QT interval* Q waves (1) And the Right blundle branch block QRS >120msQTc≤320 ms and <139 ms? 9. Early repolarisation (ST elevation, J-point Brugada-like ECG pattern High take-off and downsloping ST segment elevation followed by a negative T wave in ≥2 leads in V1–V3 elevation, J-waves Profound sinus bradycardia <30 BPM or sinus pauses ≥ 3 s or terminal QRS slurring) Atrial tachyarrhythmias Supraventricular tachycardia, atrial-fibrillation, atrial-flutter 10. Convex (‘domed’) ST segment elevation Premature ventricular contractions ≥2 PVCs per 10 s tracing combined with T-wave inversion in leads V1–V4 Ventricular arrhythmias Couplets, triplets and non-sustained ventricular in black/African athletes tachycardia Drezner JA, Ackerman MJ, Anderson J, et al. Br J Sports Med 2013;47:122–124. (1) In Seattle Criteria normal o abnormal findings in athletes ▪ The author have omitted mention of Complete Right bundle branch block QRS ≥120 ms and < 140 ms. I send to author a letter about this point about the implication of this and respond by mail “Dear Dr. Ibarrola, Thank you for the note. I appreciate your comments regarding RBBB. I think the pre-test probability that complete RBBB represents disease in most asymptomatic athlete populations is very low. Thus, in most settings I don’t think RBBB has a high positive predictive value and will not be a good distinguisher of disease. You bring up an important point that was not addressed in the Seattle summit papers -- that RBBB in countries with a high prevalence of Chagas disease should be considered abnormal. This will be considered in any future revisions to the criteria.” Response by Jonathan Drezner, MD This omitting affected papers compared to ESC recommendation compared with the Seattle Criteria. The complete RBBB have present in 1% of athletes (Pelliccia et al. EHJ 2007) but is normal o abnormal findings in athletes? In countries with Chagas disease, if reasonable? Affected this the support of better false positive in comparative paper’s? Interpretation of the athlete’s electrocardiogram Domenico Corrado et al. Improving the interpretation of the athlete’s Electrocardiogram. European Heart Journal (2013) 34, 3606–3609 Electrocardiographic Findings in athletes normal variants GROUP 1 Athletes normal variants Increased vagal tone Changes of increased cavity dimensions and wall thickness Sinus bradycardia (≥ 30 bpm). P wave must have a normal axis in the frontal plane (0–90°s) Male 27 years old. Rugby player. Sinus bradycardia 41 bpm Sinus arrhythmia Female 14 years old. Voley. 64 BPM. Sinus arrythmia Ectopic atrial rhythm: P waves are present but are a different morphology compared to the sinus P wave, negative in the inferior leads (II, III and aVF) Junctional escape rhythm or nodal rhythm Male 15 years old. Rugby player. Asyntomatic. Nodal rhytmin First-degree AV block: PR interval is prolonged (>200 ms) 27 years old 23 years old 2011 2015 Male, Rugby player, asymtomatic with BAV 1er grade 0,24 ms Second-degree AV block: Mobitz type I (Wenckebach) Male 32 years old. Asymtomatic. Intensive Spining. Early repolarization: concave ST segment elevation in the precordial leads. New definitions of Early Repolarization Types 1, 3 and 5 all have an elevated ST amplitude ≥0.1 mV with or without a notch or slur while Types 2 and 4 have the peak of a notch or onset of a slur ≥0.1 mV but without ST elevation. Peter W. Macfarlane. J wave patterns — morphology, prevalence and nomenclature. J Electrocardiol. 2013 Nov-Dec;46(6):505-9 Early repolarization Isolated QRS voltage criteria for LVH for Sokolow- Lyon criterion Incomplete right bundle branch block Male 17 years. IRBBB Abnormal electrocardiographic findings in athletes GROUP 2 Mimics incomplete Right bundle branch block ▪ Abnormal IRBBB pattern associated with other ECG abnormalities, T wave inversion involving the mid-precordial leads to V1–V3, prolonged S wave upstrokein individuals >14 years of age, low limb-lead voltages, prolonged S wave upstroke and/or premature ventricular beats with a left bundle branch block (LBBB) morphology and Epsilon waves in ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY ▪ Brugada-ECG pattern, which is characterized by a high take-off and downsloping ST segment elevation followed by a negative T wave in ≥2 leads in V1–V3. ‘J wave’ reflects early repolarisation with J point elevation and a high take-off with downsloping ST segment followed by a negative T wave Criteria for diagnosis of ARVC/D 1. Family history Major ▪ Familial disease confirmed at necropsy or surgery. Minor ▪ Family history of premature sudden death (<35 years of age) due to suspected ARVC/D. ▪ Family history (clinical diagnosis based on present criteria). 2. ECG depolarization/conduction abnormalities Major ▪ Epsilon waves or localized prolongation (>110 ms) of QRS complex in right precordial leads (V1-V3). Minor ▪ Late potentials on signal-averaged ECG. 3. ECG repolarization abnormalities ▪ Minor ▪ Inverted T waves in right precordial leads (V2 and V3) in people >12 years of age and in absence of right bundle branch block. 4. Arrhythmias Minor ▪ Sustained or nonsustained left bundle branch block-type ventricular tachycardia documented on ECG or Holter monitoring or during exercise testing. ▪ Frequent ventricular extrasystoles (>1000/24 h on Holter monitoring). 5. Global or regional dysfunction and structural alterations* Major ▪ Severe dilatation and reduction of RV ejection fraction with no or mild LV involvement. ▪ Localized RV aneurysms (akinetic or dyskinetic areas with diastolic bulgings). Severe segmental dilatation of RV. Minor ▪ Mild global RV dilatation or ejection fraction reduction with normal LV. ▪ Mild segmental dilatation of RV. ▪ Regional RV hypokinesia. 6. Tissue characteristics of walls ▪ Major ▪ Fibro-fatty replacement of myocardium on endomyocardial biopsy. ▪ * Detected by echocardiography, angiography, magnetic resonance imaging, or radionuclide scintigraphy. Modified from McKenna et al. BRUGADA PATTERN TYPE-1 TYPE-2 ▪ The differential diagnosis of Type-2 Brugada pattern and electrocardiogram of athletes Chevallier S, et al.
Load more

Recommended publications
  • Giant Right Atrium Or Ebstein Anomaly? Hacer Kamalı1, Abdullah Erdem1*, Cengiz Erol2 and Atıf Akçevin3
    ISSN: 2378-2951 Kamalı et al. Int J Clin Cardiol 2017, 4:104 DOI: 10.23937/2378-2951/1410104 Volume 4 | Issue 4 International Journal of Open Access Clinical Cardiology CASE REPORT Giant Right Atrium or Ebstein Anomaly? Hacer Kamalı1, Abdullah Erdem1*, Cengiz Erol2 and Atıf Akçevin3 1Department of Pediatric Cardiology, Istanbul Medipol University, Turkey 2Department of Radiology, Istanbul Medipol University, Turkey 3Department of Cardiovascular Surgery, Istanbul Medipol University, Turkey *Corresponding author: Abdullah Erdem, Associate Professor of Pediatric Cardiology, Department of Pediatric Cardiology, Istanbul Medipol University, Istanbul, Turkey, Tel: +905-0577-05805, Fax: +90212467064, E-mail: drabdullaherdem@ hotmail.com partment for exercise intolerance. She had been diag- Abstract nosed and followed up as Ebstein anomaly for ten years. Many acquired and congenital pathologies could cause en- Her heart rate was 75/min with normal jugular venous largement of Right Atrium (RA). In rare pathologies we couldn’t find an obvious reason for enlargement of RA. Sometimes it pressure. Findings of lung examination were normal. leads to misdiagnosis if we try to explain an unknown pa- Auscultation of heart revealed a 2/6 systolic murmur on thology with well known pathology. In this article we de- the lower left edge of the sternum. On abdominal ex- scribe a woman who presented with giant enlargement of amination, there was no organomegaly. Arterial Oxygen the RA misdiagnosed as Ebstein anomaly. Cardiac MRI is highly helpful for differential diagnosis of these kinds of atrial Saturation (SpO2) was 98%. Electrocardiography (ECG) pathologies. Although it is rare, giant RA should be consid- revealed absence of atrial fibrillation, the rhythm was ered in differential diagnosis of huge RA without an obvious sinus but there was right axis deviation and right bundle cause.
    [Show full text]
  • Clinical Manifestation and Survival of Patients with I Diopathic Bilateral
    ORIGINAL ARTICLE Clinical Manifestation and Survival of Patients with Mizuhiro Arima, TatsujiI diopathicKanoh, Shinya BilateralOkazaki, YoshitakaAtrialIwama,DilatationAkira Yamasaki and Sigeru Matsuda Westudied the histories of eight patients who lacked clear evidence of cardiac abnormalities other than marked bilateral atrial dilatation and atrial fibrillation, which have rarely been dis- cussed in the literature. From the time of their first visit to our hospital, the patients' chest radio- graphs and electrocardiograms showed markedly enlarged cardiac silhouettes and atrial fibrilla- tion, respectively. Each patient's echocardiogram showed a marked bilateral atrial dilatation with almost normal wall motion of both ventricles. In one patient, inflammatory change was demonstrated by cardiac catheterization and endomyocardial biopsy from the right ventricle. Seven of our eight cases were elderly women.Over a long period after the diagnosis of cardiome- galy or arrhythmia, diuretics or digitalis offered good results in the treatment of edema and congestion in these patients. In view of the clinical courses included in the present study, we conclude that this disorder has a good prognosis. (Internal Medicine 38: 112-118, 1999) Key words: cardiomegaly, atrial fibrillation, elder women,good prognosis Introduction echocardiography. The severity of mitral and tricuspid regur- gitation was globally assessed by dividing into three equal parts Idiopathic enlargement of the right atrium was discussed by the distance from the valve orifice. The regurgitant jet was de- Bailey in 1955(1). This disorder may be an unusual congenital tected on color Doppler recording in the four-chamber view malformation. A review of the international literature disclosed and classified into one of the three regions (-: none, +: mild, that although several cases have been discussed since Bailey's ++:moderate, +++: severe).
    [Show full text]
  • Young Adults. Look for ST Elevation, Tall QRS Voltage, "Fishhook" Deformity at the J Point, and Prominent T Waves
    EKG Abnormalities I. Early repolarization abnormality: A. A normal variant. Early repolarization is most often seen in healthy young adults. Look for ST elevation, tall QRS voltage, "fishhook" deformity at the J point, and prominent T waves. ST segment elevation is maximal in leads with tallest R waves. Note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2- 6 is concave upwards, another characteristic of this normal variant. Characteristics’ of early repolarization • notching or slurring of the terminal portion of the QRS wave • symmetric concordant T waves of large amplitude • relative temporal stability • most commonly presents in the precordial leads but often associated with it is less pronounced ST segment elevation in the limb leads To differentiate from anterior MI • the initial part of the ST segment is usually flat or convex upward in AMI • reciprocal ST depression may be present in AMI but not in early repolarization • ST segments in early repolarization are usually <2 mm (but have been reported up to 4 mm) To differentiate from pericarditis • the ST changes are more widespread in pericarditis • the T wave is normal in pericarditis • the ratio of the degree of ST elevation (measured using the PR segment as the baseline) to the height of the T wave is greater than 0.25 in V6 in pericarditis. 1 II. Acute Pericarditis: Stage 1 Pericarditis Changes A. Timing 1. Onset: Day 2-3 2. Duration: Up to 2 weeks B. Findings 1.
    [Show full text]
  • EKG Workshop Texas Academy of Physician Assistants 2018 TAPA 43Rd Annual CME Conference
    EKG Workshop Texas Academy of Physician Assistants 2018 TAPA 43rd Annual CME Conference David J. Klocko, MPAS, PA-C Associate Professor and Academic Coordinator UT Southwestern Department of PA Studies Disclosures Content in this presentation is licensed under a Creative Commons Attribution 4.0 International license. David J. Klocko is receiving a stipend from TAPA to do this workshop. Objectives Review basic electrophysiology. Recognize common cardiac dysrhythmias. Recognize common conductive disorders. Review axis, bundle branch block, chamber enlargement and hypertrophy. Recognize common ECG changes associated with myocardial ischemia and infarction. Systematic Evaluation of the 12- lead EKG –Our ultimate goal ! Step Check for: LOOK AT: 1. Rhythm Rhythm Strip 2. Axis I, AvF ** 3. BBB V1, V6 4. Ischemia, Injury or I-AvL, V5-V6 Infarct V1-V4 II, III, AvF 5. Chamber II, V1 Enlargement Intervals & Segments PR interval (PRI): start of atrial depolarization to start of ventricular depolarization Normal: 0.12 – 0.20 sec QRS complex: depolarization of ventricles Normal: 0.04 – 0.11 sec When QRS >0.12 sec, think about an interventricular conduction delay Intervals & Segments ST segment: end ventricular depolarization to start of repolarization QT interval (QTI): both ventricular depolarization & repolarization Normal: 0.3 – 0.4 sec; varies with heartrate Faster heartrates….shorter QTIs; slower heartrates ….longer QTIs Heart Rate For regular rhythms, measure the interval between complexes in large boxes 300-150-100-75-60-50-43-37-33
    [Show full text]
  • Changes in Cardiac Geometry Due to Hypertrophy
    Changes in Cardiac Geometry Due to Hypertrophy By Marta Ellen Pedersen A Master’s Paper Submitted in Partial Fulfillment of The Requirements for the Degree of Master of Science in Clinical Exercise Physiology Dr. Joseph O’ Kroy Date University of Wisconsin-River Falls 2014 Introduction For any given body size, men have larger hearts than women, athletes have larger hearts than nonathletes, and often times, an enlarged heart is a symptom of an underlying disorder that is causing the heart to work harder than normal. This review will emphasize the differences between a pathologically enlarged heart and an athletically enlarged heart. Pathologically induced hypertrophy (myopathy) When heart cells get bigger, (often is the case when heart disease is present) the total heart works less efficiently. Some people suffer from conditions like hypertrophic cardiomyopathy, which includes significant heart muscle enlargement, and can be genetic or caused by high blood pressure. Cardiomyopathy decreases the size of the heart's chambers, reducing blood flow. Hypertrophy, or thickening, of the heart muscle can occur in response to increased stress on the heart. The most common causes of Cardiomyopathy are related to increased blood pressure. The extra work of pumping blood against the increased pressure causes the ventricle to thicken over time, the same way a body muscle increases in mass in response to weightlifting. Cardiomyopathy can occur in both the right and left atrium and the right and left ventricles. Blood travels through the right ventricle to the lungs. If conditions occur that decrease pulmonary circulation, extra stress can be placed on the right ventricle, and can lead to right ventricular myopathy.
    [Show full text]
  • Abnormal ECG Findings in Athletes Normal ECG
    SEATTLE CRITERIA Abnormal ECG findings in athletes These ECG findings are unrelated to regular training or expected physiologic adaptation to exercise, may suggest the presence of pathologic cardiovascular disease, and require further diagnostic evaluation. Abnormal ECG finding Definition T wave inversion > 1 mm in depth in two or more leads V2-V6, II and aVF, or I and aVL (excludes III, aVR, and V1) ST segment depression ≥ 0.5 mm in depth in two or more leads Pathologic Q waves > 3 mm in depth or > 40 ms in duration in two or more leads (except III and aVR) Complete left bundle branch block QRS ≥ 120 ms, predominantly negative QRS complex in lead V1 (QS or rS), and upright monophasic R wave in leads I and V6 Intra-ventricular conduction delay Any QRS duration ≥ 140 ms Left axis deviation -30° to -90° Left atrial enlargement Prolonged P wave duration of > 120 ms in leads I or II with negative portion of the P wave ≥ 1 mm in depth and ≥ 40 ms in duration in lead V1 Right ventricular hypertrophy R-V1 + S-V5 > 10.5 mm and right axis deviation > 120° pattern Ventricular pre-excitation PR interval < 120 ms with a delta wave (slurred upstroke in the QRS complex) and wide QRS (> 120 ms) Long QT interval* QTc ≥ 470 ms (male) QTc ≥ 480 ms (female) QTc ≥ 500 ms (marked QT prolongation) Short QT interval* QTc ≤ 320 ms Brugada-like ECG pattern High take-off and downsloping ST segment elevation followed by a negative T wave in ≥ 2 leads in V1-V3 Profound sinus bradycardia < 30 BPM or sinus pauses ≥ 3 sec Mobitz type II 2° AV block Intermittently non-conducted P waves not preceded by PR prolongation and not followed by PR shortening 3° AV block Complete heart block Atrial tachyarrhythmias Supraventricular tachycardia, atrial fibrillation, atrial flutter Premature ventricular contractions ≥ 2 PVCs per 10 second tracing Ventricular arrhythmias Couplets, triplets, and non-sustained ventricular tachycardia *The QT interval corrected for heart rate is ideally measured with heart rates of 60-90 bpm.
    [Show full text]
  • Accuracy of Electrocardiographic Criteria for Atrial Enlargement: Validation with Cardiovascular Magnetic Resonance
    Accuracy of Electrocardiographic Criteria for Atrial Enlargement: Validation with Cardiovascular Magnetic Resonance The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Tsao, Connie W., Mark E. Josephson, Thomas H. Hauser, T. David O'Halloran, Anupam Agarwal, Warren J. Manning, and Susan B. Yeon. 2008. Accuracy of electrocardiographic criteria for atrial enlargement: Validation with cardiovascular magnetic resonance. Journal of Cardiovascular Magnetic Resonance 10(1): 7. Published Version doi://10.1186/1532-429X-10-7 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:10140325 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Journal of Cardiovascular Magnetic Resonance BioMed Central Research Open Access Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance Connie W Tsao1, Mark E Josephson1, Thomas H Hauser1, T David O'Halloran1, Anupam Agarwal1,2, Warren J Manning1,3 and Susan B Yeon*1 Address: 1Harvard-Thorndike Laboratory and the Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts, USA, 2Cardiovascular and Metabolic Division, GlaxoSmithKline Pharmaceuticals, 1250 Collegeville
    [Show full text]
  • Surgical Treatment of Idiopathic Enlargement of the Right Atrium
    Hindawi Case Reports in Surgery Volume 2018, Article ID 7241309, 5 pages https://doi.org/10.1155/2018/7241309 Case Report Surgical Treatment of Idiopathic Enlargement of the Right Atrium Francesca Chiara Surace, Federica Iezzi , Massimo Colaneri, and Marco Pozzi Department of Paediatric and Congenital Cardiac Surgery and Cardiology, Azienda Ospedaliero Universitaria, Ospedali Riuniti Ancona “Umberto I-G. M. Lancisi-G. Salesi”, Ancona, Italy Correspondence should be addressed to Federica Iezzi; federicaiezzi@hotmail.it Received 25 June 2018; Accepted 26 August 2018; Published 20 September 2018 Academic Editor: Shuli Silberman Copyright © 2018 Francesca Chiara Surace et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Idiopathic enlargement of the right atrium (IERA) is a very rare abnormality. Approximately one-half (48%) of the patients with a congenital enlargement of the right atrium have no symptoms. When they occur, symptoms include shortness of breath (28% of cases), palpitations (17%), arrhythmias (12%), and in rare cases, right heart failure and extreme tiredness. We report one such case of a young man with a disproportionally enlarged right atrium. The basal transthoracic echocardiogram demonstrated a huge right atrium with a thick smoke pattern and mild tricuspid regurgitation in the absence of congenital heart disease. Magnetic resonance imaging confirmed the right atriomegaly, with initial compression of the right ventricle, and excluded congenital heart defects or absence of pericardium. The patient underwent surgical resection of the right atrial wall and the atriotomy was closed, leaving an atrial chamber of normal consistency and size.
    [Show full text]
  • Dysrhythmias
    CARDIOVASCULAR DISORDERS DYSRHYTHMIAS I. BASIC PRINCIPLES OF CARDIAC CONDUCTION DISTURBANCES A. Standard ECG and rhythm strips 1. Recordings are obtained at a paper speed of 25 mm/sec. 2. The vertical axis measures distance; the smallest divisions are 1 mm ×1 mm. 3. The horizontal axis measures time; each small division is 0.04 sec/mm. B. Normal morphology Courtesy of Dr. Michael McCrea 1. P wave = atrial depolarization a. Upright in leads I, II, III, aVL, and aVF; inverted in lead aVR b. Measures <0.10 seconds wide and <3 mm high c. Normal PR interval is 0.12–0.20 seconds. 2. QRS complex = ventricular depolarization a. Measures 0.06-0.10 seconds wide b. Q wave (1) <0.04 seconds wide and <3 mm deep (2) Abnormal if it is >3 mm deep or >1/3 of the QRS complex. c. R wave ≤7.5 mm high 3. QT interval varies with rate and sex but is usually 0.33–0.42 seconds; at normal heart rates, it is normally <1/2 the preceding RR interval. 4. T wave = ventricular repolarization a. Upright in leads I, II, V3–V6; inverted in aVR b. Slightly rounded and asymmetric in configuration c. Measures ≤5 mm high in limb leads and ≤10 mm high in the chest leads 5. U wave = a ventricular afterpotential a. Any deflection after the T wave (usually low voltage) b. Same polarity as the T wave c. Most easily detected in lead V3 d. Can be a normal component of the ECG e. Prominent U waves may indicate one of the following: (1) Hypokalemia (<3 mEq/L) (2) Hypercalcemia (3) Therapy with digitalis, phenothiazines, quinidine, epinephrine, inotropic agents, or amiodarone (4) Thyrotoxicosis f.
    [Show full text]
  • Normal P Wave, in Atrial Enlargements, Artifacts, Dextrocardia and Interatrial Blocks
    Class 6 – SOLAECE Course Normal P wave, in atrial enlargements, artifacts, dextrocardia and interatrial blocks Authors: Antonio Bayés de Luna, Andrés R. Pérez-Riera, Adrian Baranchuk, Diego Conde The authors do not report any conflict of interest regarding this presentation 1. Introduction For some authors the name “atrial abnormalities” encompass the concept of atrial enlargement and atrial blocks (Bayés de Luna 2013)( Lee 2007). In this work we will expose the ECG/VCG characteristics of both concepts, emphasizing, as it happens with ventricular hypertrophy and ventricular blocks, that often the ECG/ VCG pattern of atrial enlargement especially of left atrial enlargement (LAE) is explained by the coexistence of interatrial block (IAB). However as we will see later there are clear evidences that the pattern of IAB may exist without the association of atrial enlargement/hypertrophy. Therefore atrial blocks and atrial enlargement are separate entities that are often associated with each other. Therefore we do not consider it appropriate to use the “umbrella” term atrial abnormalities to include both concepts without distinguishing between them (Lee 2007), as some authors do (Bayés de Luna 2013: ) (Tsao 2008). Depolarization and repolarization mode of the atria and ventricles A) Atrial muscle strip Depolarization P Longitudinal Repolarization Ta P Ta B) Ventricular myocardium R Depolarization T Transversal Repolarization q s Atrial Activation Pathways A Hypothesis currently accepted B Previous hypotesis SVC SVC SPV SPV IPV A LA LA IPV SAN SAN M BB RA RA P LV LV AV node AV node RV RV IVC IVC A: Anterior internodal bundle SVC: Superior Vena Cava M: Middle internodal or Wenckebach bundle IVC: Inferior Vena Cava P: Posterior internodal or Thorel Bundle RA: Right Atrium BB: Bachmann’s Bundle LA: Left Atrium SAN: Sinoatrial Node Old or previous hypothesis B – The activation wave spreads in a radiated way through the atria, just as the waves in a lake when you throw a stone in it.
    [Show full text]
  • Statistical Analysis Plan for Primary Analysis, and Final Analysis
    NCT02993250 Janssen Pharmaceutical K.K. * Statistical Analysis Plan for Primary Analysis, and Final Analysis A Phase 2a, Multicenter, Open-label Study to Investigate the Safety, Pharmacokinetics, and Efficacy of Combination Treatment of AL-335, Odalasvir, and Simeprevir in Japanese Subjects With Chronic Hepatitis C Genotype 1 or 2 Virus Infection, With or Without Compensated Cirrhosis who are Direct-acting Antiviral Treatment-naïve Protocol 64294178HPC2003; Phase 2a AL-335, Odalasvir, TMC435(simeprevir) *This study is being conducted by Janssen Pharmaceutical K.K. in Japan. The term “sponsor” is used throughout the protocol to represent Janssen Pharmaceutical K.K. Status: Approved Date: 8 June 2018 Prepared by: Janssen Pharmaceutical K.K. Document No.: EDMS-ERI-164033457 Compliance: The study described in this report was performed according to the principles of Good Clinical Practice (GCP). Confidentiality Statement The information in this document contains trade secrets and commercial information that are privileged or confidential and may not be disclosed unless such disclosure is required by applicable law or regulations. In any event, persons to whom the information is disclosed must be informed that the information is privileged or confidential and may not be further disclosed by them. These restrictions on disclosure will apply equally to all future information supplied to you that is indicated as privileged or confidential. 1 Approved, Date: 8 June 2018 NCT02993250 AL-335, Odalasvir, TMC435(simeprevir) Statistical Analysis Plan
    [Show full text]
  • The P Wave: Indicator of Atrial Enlargement - Print Article - JAAPA
    Marquette University e-Publications@Marquette Physician Assistant Studies Faculty Research and Physician Assistant Studies, Department Publications 8-12-2010 The P aW ve: Indicator of Atrial Enlargement Patrick Loftis Marquette University, patrick.loftis@marquette.edu Accepted version. Journal of the American Academy of Physician Assistants (August 2010). Permalink.© 2010, American Academy of Physician Assistants and Haymarket Media Inc. Used with permission. The P wave: Indicator of atrial enlargement - Print Article - JAAPA http://www.jaapa.com/the-p-wave-indicator-of-atrial-enlargement/printart... << Return to The P wave: Indicator of atrial enlargement James F. Ginter, MPAS, PA-C, Patrick Loftis, PA-C, MPAS, RN August 12 2010 Once you've determined that a P wave precedes each QRS complex, you must scrutinize the P wave for contour and size. The normal P wave is less than 0.12 seconds in duration, and the largest deflection, whether positive or negative, should not exceed 2.5 mm. An abnormal P wave may indicate atrial enlargement. Atrial depolarization follows the discharge of the sinus node. Normally depolarization occurs first in the right atrium and then in the left atrium. Atrial enlargement is best observed in the P waves of leads II and V1. Lead II is oriented parallel to the flow of current through the atrium and is the main P wave vector. V1 is oriented perpendicular to the flow of current through the atrium. This results in a biphasic P wave, in which the first peak represents depolarization of the right atrium and the second peak represents depolarization of the left atrium, allowing for easy differentiation between the atria.
    [Show full text]